Blood Gas Interpretation
Transcript of Blood Gas Interpretation
![Page 1: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/1.jpg)
Blood Gas Interpretation
![Page 2: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/2.jpg)
Before beginning…
Allen’s test for radial and ulnar artery Common errors of arterial blood sampling
Air in sample: PCO2↓, pH↑, PO2↨Venous mixture: PCO2↑, pH↓, PO2↓Excess anticoagulant (dilution): PCO2↓, pH↑, PO2↨
(RARE)Metabolic effects: PCO2↑, pH↓, PO2↓
Simultaneous electrolytes panel
![Page 3: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/3.jpg)
Normal Range PHa = 7.35-7.45 (7.40) PHv = 7.31-7.41 (7.36) PaCO2 = 35-45 mmHg (40 mmHg) PvCO2= 41-51 mmHg (46 mmHg) HCO3
- = 22-26 mEq/L (24 mEq/L) SaO2 = 95%-100% (97%) SvO2 = 68%-77% (75%)
![Page 4: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/4.jpg)
Bicarbonate Buffering System
CO2 + H2O H2CO3 H+ + HCO3-
Oral intake
Kidney
Metabolism
Oral intake
Kidney
Stomach
Metabolism
Lung
![Page 5: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/5.jpg)
Henderson-Hasselbalch Equation
pH = 6.1 + log ([HCO3-]/0.0301xPCO2)
![Page 6: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/6.jpg)
Determinants of CO2 in the alveolus
PaCO2 = (0.863) x (VCO2/VA)
(VA = VE – VD )
Physiologic dead space = anatomic dead space + alveolar dead space
![Page 7: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/7.jpg)
Renal Regulation of Bicarbonate
“Reabsorption“ of filtered HCO3- (4000 mmol/day)
Formation of titratable acid (4000 mmol/day H+) Excretion of NH4+ in the urine 80-90% of HCO3
- : reabsorbed in the proximal tubule
Distal tubule: reabsorption of remained bicarbonate and secretion of hydrogen ion
![Page 8: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/8.jpg)
STEPS OF ABG INTERPRETATION
Classification
Type of disorder (Resp. or Metab.) Calculations
Calculate Compensation and Gaps Confirmation
Patient History, baseline, check for accuracy
![Page 9: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/9.jpg)
Respiratory acidosis
pH PaCo2 HC03
normal
Respiratory
Alkalosis
normal
Metabolic Acidosis
normal
Metabolic Alkalosis
normal
![Page 10: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/10.jpg)
So• PaCO2 > 44 with a pH < 7.35 represents a respiratory acidosis
*PaCO2 < 36 with a pH > 7.45 represents a respiratory alkalosis
For a primary respiratory problem, pH and paCO2 move in the opposite directionFor each deviation in paCO2 of 10 mm Hg in
either direction, 0.08 pH units change in the opposite direction
![Page 11: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/11.jpg)
And
*HCO3 < 22 with a pH < 7.35 represents a metabolic acidosis
*HCO3 > 26 with a pH > 7.45 represents a metabolic alkalosis
For a primary metabolic problem, pH and HCO3 are in the same direction, and paCO2 is also in the same direction
![Page 12: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/12.jpg)
Compensation
The body’s attempt to return the acid/base status to normal (i.e. pH closer to 7.4)
Primary Problem Compensation
respiratory acidosis metabolic alkalosis
respiratory alkalosis metabolic acidosis
metabolic acidosisrespiratory alkalosis
metabolic alkalosis respiratory acidosis
![Page 13: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/13.jpg)
Expected Compensation
Respiratory acidosis Acute – the pH decreases 0.08 units for every 10 mm
Hg increase in paCO2; HCO3 0.1-1 mEq/liter per 10 mm Hg paCO2
Chronic – the pH decreases 0.03 units for every 10 mm Hg increase in paCO2; HCO3 1.1-3.5 mEq/liter per 10 mm Hg paCO2
![Page 14: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/14.jpg)
Expected Compensation
Respiratory alkalosis Acute – the pH increases 0.08 units for every 10 mm Hg
decrease in paCO2; HCO3 0-2 mEq/liter per 10 mm Hg paCO2
Chronic - the pH increases 0.17 units for every 10 mm Hg decrease in paCO2; HCO3 2.1-5 mEq/liter per 10 mm Hg paCO2
![Page 15: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/15.jpg)
Expected Compensation
Metabolic acidosis paCO2 = 1.5(HCO3) + 8 (2)
paCO2 1-1.5 per 1 mEq/liter HCO3
Metabolic alkalosis paCO2 = 0.7(HCO3) + 20 (1.5)
paCO2 0.5-1.0 per 1 mEq/liter HCO3
![Page 16: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/16.jpg)
Metabolic Acidosis
Causes: Indogenous acid production (lactic acidosis, k
etoacidosis) Indogenous acid accumulation (renal failure) Loss of bicarbonate (diarrhea) High anion gap Normal (hyperchloremic )
![Page 17: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/17.jpg)
Pathophysiologic Effect of Metabolic Acidosis
Kussmaul respiration Central vasoconstriction pulmonary edema Depressed CNS function Glucose intolerance
![Page 18: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/18.jpg)
Anion Gap
AG = Na+ - (Cl- + HCO3-) Unmeasured anions in plasma (normally 10 to
12 mmol/L) Anionic proteins, phosphate, sulfate, and
organic anions Correction: if albumin < 4
Albumin ↓1 AG ↓ 2.5
![Page 19: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/19.jpg)
Anion Gap
Increase Increased unmeasured
anions Decreased unmeasured
cations (Ca++, K+, Mg++) Increase in anionic
albumin
Decrease Increase in unmeasured cations Addition of abnormal cations Reduction in albumin concentra
tion Decrease in the effective anioni
c charge on albumin by acidosis
Hyperviscosity and severe hyperlipidemia ( underestimation of sodium and chloride concentration)
![Page 20: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/20.jpg)
![Page 21: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/21.jpg)
Causes of High-Anion-Gap Metabolic Acidosis
Lactic acidosis Toxins
Ketoacidosis Ethylene glycol
Diabetic Methanol
Alcoholic Salicylates
Starvation Renal failure (acute and chronic)
![Page 22: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/22.jpg)
Causes of Non-Anion-Gap Acidosis
I. Gastrointestinal bicarbonate loss A. Diarrhea B. External pancreatic or small-bowel drainage C. Ureterosigmoidostomy, jejunal loop, ileal loop D. Drugs 1. Calcium chloride (acidifying agent) 2. Magnesium sulfate (diarrhea) 3. Cholestyramine (bile acid diarrhea)II. Renal acidosis A. Hypokalemia 1. Proximal RTA (type 2) 2. Distal (classic) RTA (type 1) B. Hyperkalemia 1. Generalized distal nephron dysfunction (type 4 RTA) a. Mineralocorticoid deficiency b. Mineralocorticoid resistance c. ØNa+ delivery to distal nephron d. Tubulointerstitial disease e. Ammonium excretion defectIII. Drug-induced hyperkalemia (with renal insufficiency) A. Potassium-sparing diuretics (amiloride, triamterene, spironolactone) B. Trimethoprim C. Pentamidine D. Angiotensin-converting enzyme inhibitors and AT-II receptor blockers E. Nonsteroidal anti-inflammatory drugs F. CyclosporineIV. Other A. Acid loads (ammonium chloride, hyperalimentation) B. Loss of potential bicarbonate: ketosis with ketone excretion C. Expansion acidosis (rapid saline administration) D. Hippurate E. Cation exchange resins
![Page 23: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/23.jpg)
Mixed Metabolic Disorders:
Bicarbonate Gap: BG= Patient HCO3+ΔAG Normal BG=24 (20-28) 24 AG met. Acidosis <20 AG met Acid. + non AG met. Acid. >28 AG met Acid. + Met. Alk
![Page 24: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/24.jpg)
Metabolic Alkalosis
Net gain of [HCO3- ]
Loss of nonvolatile acid (usually HCl by vomiting) from the extracellular fluid
Kidneys fail to compensate by excreting HCO3-
(volume contraction, a low GFR, or depletion of Cl- or K+)
![Page 25: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/25.jpg)
Causes of Metabolic Alkalosis
I. Exogenous HCO3- loads A. Acute alkali administration B. Milk-alkali syndromeII. Effective ECFV contraction, normotension, K+ deficiency, and secondary hyperreninemic hyperaldosteronism A. Gastrointestinal origin 1. Vomiting 2. Gastric aspiration 3. Congenital chloridorrhea 4. Villous adenoma 5. Combined administration of sodium polystyrene sulfonate (Kayexalate) and aluminum hydroxide B. Renal origin 1. Diuretics 2. Edematous states 3. Posthypercapnic state 4. Hypercalcemia/hypoparathyroidism 5. Recovery from lactic acidosis or ketoacidosis 6. Nonreabsorbable anions including penicillin, carbenicillin 7. Mg2+ deficiency 8. K+ depletion 9. Bartter's syndrome (loss of function mutations in TALH) 10. Gitelman's syndrome (loss of function mutation in Na+-Cl- cotransporter in DCT)
![Page 26: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/26.jpg)
Causes of Metabolic Alkalosis
III. ECFV expansion, hypertension, K+ deficiency, and mineralocorticoid excess A. High renin 1. Renal artery stenosis 2. Accelerated hypertension 3. Renin-secreting tumor 4. Estrogen therapy B. Low renin 1. Primary aldosteronism a. Adenoma b. Hyperplasia c. Carcinoma 2. Adrenal enzyme defects a. 11b-Hydroxylase deficiency b. 17a-Hydroxylase deficiency 3. Cushing's syndrome or disease 4. Other a. Licorice b. Carbenoxolone c. Chewer's tobacco d. Lydia Pincham tabletsIV. Gain of function mutation of renal sodium channel with ECFV expansion, hypertension, K+ deficiency, and hyporeninemic-hypoaldosteronism A. Liddle's syndrome
![Page 27: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/27.jpg)
Respiratory Acidosis
Severe pulmonary disease Respiratory muscle fatigue Abnormal ventilatory control Acute vs. Chronic (> 24 hrs)
![Page 28: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/28.jpg)
Respiratory Acidosis
Acute: anxiety, dyspnea, confusion, psychosis, and hallucinations and coma
Chronic: sleep disturbances, loss of memory, daytime somnolence, personality changes, impairment of coordination, and motor disturbances such as tremor, myoclonic jerks, and asterixis
Headache: vasocontriction
![Page 29: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/29.jpg)
Respiratory Acid-Base Disorders
II. Acidosis A. Central 1. Drugs (anesthetics, morphine, sedatives) 2. Stroke 3. Infection B. Airway 1. Obstruction 2. Asthma C. Parenchyma 1. Emphysema 2. Pneumoconiosis 3. Bronchitis 4. Adult respiratory distress syndrome 5. Barotrauma D. Neuromuscular 1. Poliomyelitis 2. Kyphoscoliosis 3. Myasthenia 4. Muscular dystrophies E. Miscellaneous 1. Obesity 2. Hypoventilation 3. Permissive hypercapnia
![Page 30: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/30.jpg)
![Page 31: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/31.jpg)
Respiratory Alkalosis
Strong ventilatory stimulus with alveolar hyperventilation
Consuming HCO3-
> 2-6 hrs: renal compensation (decrease NH4+/acid excretion and bicarbonate re-absorption)
![Page 32: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/32.jpg)
Respiratory Alkalosis
Reduced cerebral blood flow dizziness, mental confusion, and seizures
Minimal cardiovascular effect in normal health Cardiac output and blood pressure may fall in
mechanically ventilated patients Bohr effect: left shift of hemoglobin-O2 dissociation
curve tissue hypoxia (arrhythmia) intracellular shifts of Na+, K+, and PO4
- and reduces free [Ca2+]
![Page 33: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/33.jpg)
Respiratory Acid-Base Disorders
I. Alkalosis A. Central nervous system stimulation 1. Pain 2. Anxiety, psychosis 3. Fever 4. Cerebrovascular accident 5. Meningitis, encephalitis 6. Tumor 7. Trauma B. Hypoxemia or Tissue hypoxia 1. High altitude, ØPaCO2 2. Pneumonia, pulmonary edema 3. Aspiration 4. Severe anemia C. Drugs or hormones 1. Pregnancy, progesterone 2. Salicylates 3. Nikethamide D. Stimulation of chest receptors 1. Hemothorax 2. Flail chest 3. Cardiac failure 4. Pulmonary embolism E. Miscellaneous 1. Septicemia 2. Hepatic failure 3. Mechanical hyperventilation 4. Heat exposure 5. Recovery from metabolic acidosis
![Page 34: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/34.jpg)
Stepwise Approach
Do comprehensive history taking and physical examination
Assess accuracy of data Direction of pH: always indicates the primary
disturbance Calculate the expected compensation Second or third disorders
![Page 35: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/35.jpg)
N
Respiratory alkalosis
Metabolic alkalosis
Metabolic acidosis
Respiratory acidosis
7.4
7.6
7.2
pH
30 40 50
PCO2 (mmHg)
Determination of primary acid-base disorders
![Page 36: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/36.jpg)
![Page 37: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/37.jpg)
Compensatory Mechanisms
Respiratory compensationComplete within 24 hrs
Metabolic compensationComplete within several days
Both the respiratory or renal compensation almost never over-compensates
![Page 38: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/38.jpg)
Prediction of Compensatory Responses on SimpleAcid-Base Disturbances
Disorder Prediction of Compensation
Metabolic acidosis PaCO2 = (1.5x HCO3-) + 8 or
PaCO2 will ↓ 1.25 mmHg per mmol/L ↓ in [HCO3-] or
PaCO2 = [HCO3-] + 15
Metabolic alkalosis PaCO2 will ↑ 0.75 mmHg per mmol/L ↑ in [HCO3-] or
PaCO2 will ↑ 6 mmHg per 10-mmol/L ↑ in [HCO3-] or
PaCO2 = [HCO3-] + 15
Respiratory alkalosis
Acute [HCO3-] will ↓ 2 mmol/L per 10-mmHg ↓ in PaCO2
Chronic [HCO3-] will ↓ 4 mmol/L per 10-mmHg ↓ in PaCO2
Respiratory acidosis
Acute [HCO3-] will ↑ 1 mmol/L per 10-mmHg ↑ in PaCO2
Chronic [HCO3-] will ↑ 4 mmol/L per 10-mmHg ↑ in PaCO2
![Page 39: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/39.jpg)
![Page 40: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/40.jpg)
Mixed Acid Base Disorders
Primary
Secondary
Respiratory acidosis
Respiratory alkalosis
Metabolic acidosis
Metabolic alkalosis
Respiratory acidosis
Respiratory alkalosis
Metabolic acidosis
Metabolic alkalosis
![Page 41: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/41.jpg)
Mechanisms of Hypoxemia
Inadequate inspiratory partial pressure of oxygen
Hypoventilation Right to left shunt Ventilation-perfusion mismatch Incomplete diffusion equilibrium
![Page 42: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/42.jpg)
Assessment of Gas Exchange
Alveolar-arterial O2 tension difference A-a gradient PAO2-PaO2
PAO2 = FIO2(PB - PH2O) - PaCO2/RQ* arterial-Alveolar O2 tension ratio
PaO2/PAO2
arterial-inspired O2 ratio PaO2/FIO2
P/F ratio*RQ=respiratory quotient= 0.8
![Page 43: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/43.jpg)
Summary
First, does the patient have an acidosis or an alkalosis Look at the pH
Second, what is the primary problem – metabolic or respiratoryLook at the pCO2
If the pCO2 change is in the opposite direction of the pH change, the primary problem is respiratory
![Page 44: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/44.jpg)
Summary
Third, is there any compensation by the patient - do the calculationsFor a primary respiratory problem, is the pH
change completely accounted for by the change in pCO2
if yes, then there is no metabolic compensation if not, then there is either partial compensation or
concomitant metabolic problem
![Page 45: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/45.jpg)
Summary
For a metabolic problem, calculate the expected pCO2
if equal to calculated, then there is appropriate respiratory compensation
if higher than calculated, there is concomitant respiratory acidosis
if lower than calculated, there is concomitant respiratory alkalosis
![Page 46: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/46.jpg)
Summary
Next, don’t forget to look at the effectiveness of oxygenation, (and look at the patient)your patient may have a significantly increased
work of breathing in order to maintain a “normal” blood gas
metabolic acidosis with a concomitant respiratory acidosis is concerning
![Page 47: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/47.jpg)
Case 1
Little Boy: He suffers a significant depression of mental status and respiration. You see him in
the ER 3 hours after ingestion with a respiratory rate of 4. A blood gas is obtained (after doing the ABC’s, of course). It shows
pH = 7.16, pCO2 = 70, HCO3 = 22
![Page 48: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/48.jpg)
Case 1
What is the acid/base abnormality?
1. Uncompensated metabolic acidosis
2. Compensated respiratory acidosis
3. Uncompensated respiratory acidosis
4. Compensated metabolic alkalosis
![Page 49: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/49.jpg)
Case 2
Little girl has had vomiting and diarrhea for 3 days. In her mom’s words, “She can’t keep anything down and she’s runnin’ out.” She
has had 1 wet diaper in the last 24 hours. She appears cool to touch with a prolonged
capillary refill time. her blood gas reveals: pH=7.34, pCO2=26, HCO3=12
![Page 50: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/50.jpg)
Case 2
What is the acid/base abnormality?
1. Uncompensated metabolic acidosis
2. Compensated respiratory alkalosis
3. Uncompensated respiratory acidosis
4. Compensated metabolic acidosis
![Page 51: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/51.jpg)
Case 2
Compensated metabolic acidosis The prolong history of fluid loss through diarrhea has
caused a metabolic acidosis. The mechanisms probably are twofold. First there is lactic acid production from the hypovolemia and tissue hypoperfusion. Second, there may be significant bicarbonate losses in the stool. The body has compensated by “blowing off” the CO2 with increased respirations.
![Page 52: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/52.jpg)
Case 3PH 7.52 ,PaCO2 30, HCO3 21,PaO2 62
Na 142, Cl 98:
* Interpretation• Calculate Anion Gap• Calculate Bicarbonate Gap• Oxygenation Status
![Page 53: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/53.jpg)
Oxygenation
Poor diffusion across alveolar membrane Small pressure gradient between PAO2 and
PaO2
Large alveolar area is required for gas transfer
Hemoglobin carries the majority of oxygen in the blood
![Page 54: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/54.jpg)
![Page 55: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/55.jpg)
Oxygenation
Ventilation and alveolar disease Ventilation↓PAO2 ↓PaO2 ↓, combined PCO2↑
Alveolar disease Reduced alveolar area Thickened alveolar membrane V/Q mismatch Shunt
![Page 56: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/56.jpg)
Alveolar-arterial Oxygen Gradient
PAO2 = FiO2 (PB-PH2O) – PCO2/R
= 0.21(760-47) – 40/0.8
= 100
R: respiratory quotient
P(A-a)O2 = PAO2 – PaO2
(= Age x 0.4)
![Page 57: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/57.jpg)
![Page 58: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/58.jpg)
Oxygen Content and Saturation
O2 content = 1.34 x Hb x Saturation + 0.0031xPO2
![Page 59: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/59.jpg)
Pulse Oximeters
Percentage of oxygenated hemoglobin in blood Absorption of light in the red and infra-red spectra Continuous monitor Accurate (3%) at high saturation, less below 80% Insensitive around the normal PO2
COHb and MetHb
![Page 60: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/60.jpg)
Clinical Example 1
72 y/o male, COPD with acute exacerbation Under O2 2L/min
pH 7.44, PCO2 54, PO2 60, HCO3 36
Metabolic alkalosis with respiratory compensation
Mixed respiratory acidosis
![Page 61: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/61.jpg)
Clinical Example 2
30 y/o male, sudden onset dyspnea Room air 7.33/24/111/12 Metabolic acidosis Respiratory compensation Normal A-a O2 gradient O2↑: hyperventilation
![Page 62: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/62.jpg)
Clinical Example 3
70 y/o male, acute hemoptysis and dyspnea Room air 7.50/31/88/24 Respiratory alkalosis Not been renal compensated yet Normal PO2, but A-a O2 gradient↑
![Page 63: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/63.jpg)
Clinical Example 4
18 y/o female, chest tightness and dyspnea for 4 hrs RR 28/min, distressed, widespread wheezing O2 mask 6L/min 7.31/49/115/26 Respiratory acidosis Normal bicarbonate acute May have problems with oxygenation
![Page 64: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/64.jpg)
Clinical Example 5
37 y/o female, mild asthma history Wheezes for 3 weeks, increasing chest tightness and dyspnea f
or 24 hrs, call for ambulance with Oxygen use RR 18/min, anxious and distressed Room air 7.37/43/97/27 Normal? r/o CO2 retention Low A-a O2: Oxygen use in the ambulance
![Page 65: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/65.jpg)
Clinical Example 6
19 y/o male, Duchenne muscular dystrophy on wheelchair for 7 yrs
No previous respiratory problems but frequent UTI Room air 7.21/81/44/36 Respiratory acidosis Metabolic compensation Normal A-a O2 pure ventilatory failure
![Page 66: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/66.jpg)
Clinical Example 7
57 y/o male, smoker, one week URI then 36 hrs productive cough, fever and dyspnea
RR 36/min, distressed, CXR: RLL pneumonia 7.33/27/51/22, 2L/min 7.34/32/58/24, 10L/min mask Early metabolic acidosis Severe hypoxemic respiratory failure Intra-pulmonary shunting
![Page 67: Blood Gas Interpretation](https://reader031.fdocuments.net/reader031/viewer/2022013102/54771b10b4af9f58108b4616/html5/thumbnails/67.jpg)
Thank you for your attention